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Inhibition of STING-induced mitochondrial Drp1/N-GSDMD-mediated MtDNA release alleviates Sepsis-induced lung injury
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Inhibition of STING-induced mitochondrial Drp1/N-GSDMD-mediated MtDNA release alleviates Sepsis-induced lung injury
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Inhibition of STING-induced mitochondrial Drp1/N-GSDMD-mediated MtDNA release alleviates Sepsis-induced lung injury
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Journal Article
Inhibition of STING-induced mitochondrial Drp1/N-GSDMD-mediated MtDNA release alleviates Sepsis-induced lung injury
2025
Overview
The stimulator of interferon genes (STING) pathway serves as a crucial nexus in inflammatory responses and cell death. Despite its role in Mitochondria-Endoplasmic Reticulum Contact (MERC), the mechanistic contributions to inflammatory outcomes remain poorly understood. In clinical acute respiratory distress syndrome (ARDS) models of COVID-19 infection and animal models of LPS-induced acute lung injury (ALI), the STING pathway is closely associated with the pyroptosis pathway. The macrophage STING-N-GSDMD-mtDNA positive feedback loop, upon LPS challenge, induces inflammatory responses and pyroptosis. The GSDMD inhibitor disulfiram (DSF) specifically abrogates the N-terminal portion of GSDMD anchored to the mitochondrial membrane. Furthermore, macrophage STING mediates the direct interaction between Drp1 and N-GSDMD on mitochondrial membrane by regulating mitochondrial calcium, linking mitochondrial fission to the induction of inflammatory responses. Targeting STING-mediated mitochondrial homeostasis, both genetically and pharmacologically, may play a protective role in preventing and treating sepsis-induced acute lung injury. Overall, our study posits that STING deficiency mitigates the cooperative interaction between N-GSDMD and Drp1 in mediating mitochondrial permeabilization and rupture following LPS challenge, paving the way for further investigations into inflammation and pyroptosis.
Graphical abstract
Publisher
Springer International Publishing,Springer Nature B.V,Springer
Subject
/ Acute Lung Injury - metabolism
/ Acute Lung Injury - pathology
/ acute respiratory distress syndrome
/ Animals
/ Biomedical and Life Sciences
/ calcium
/ COVID-19
/ DNA, Mitochondrial - genetics
/ DNA, Mitochondrial - metabolism
/ Endoplasmic Reticulum-Mitochondria contact
/ Genes
/ Humans
/ Intracellular Signaling Peptides and Proteins - antagonists & inhibitors
/ Intracellular Signaling Peptides and Proteins - metabolism
/ Lipopolysaccharides - toxicity
/ Lungs
/ Male
/ Membrane Proteins - genetics
/ Membrane Proteins - metabolism
/ Mice
/ Original
/ Proteins
/ Respiratory distress syndrome
/ Roles
/ Sepsis
